Muscle-coll-specific enhancer sequence Myogenic ЬHLH proteln Binding of proteln heterodimer activates the gene. (a) Binding of a myogenic BHLH proteln-E heterodimer to a muscle-cell-specific enhancer Muscle-cell-specific enhancer sequence Myogenic Id ЬHLH Heterodimer is unable to bind- proteln gene is not activated. protein (b) Inability of a myogenic BHLH proteln-ld heterodimer to bind to the DNA

Muscle-coll-specific enhancer sequence Myogenic ЬHLH proteln Binding of proteln heterodimer activates the gene. (a) Binding of a myogenic BHLH proteln-E heterodimer to a muscle-cell-specific enhancer Muscle-cell-specific enhancer sequence Myogenic Id ЬHLH Heterodimer is unable to bind- proteln gene is not activated. protein (b) Inability of a myogenic BHLH proteln-ld heterodimer to bind to the DNA

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter29: Transcription And The Regulation Of Gene Expression

Section: Chapter Questions

Problem 7P

See similar textbooks

Similar questions

Identify the ligand that bind to uniprotkb-P39086, the type of allostery, and describe the general function of the protein
It is not an easy matter to assign particular func-tions to specific components of the basal lamina, sincethe overall structure is a complicated composite materialwith both mechanical and signaling properties. Nidogen,for example, cross-links two central components of thebasal lamina by binding to the laminin γ-1 chain and totype IV collagen. Given such a key role, it was surprisingthat mice with a homozygous knockout of the gene fornidogen-1 were entirely healthy, with no abnormal phe-notype. Similarly, mice homozygous for a knockout of thegene for nidogen-2 also appeared completely normal. Bycontrast, mice that were homozygous for a defined muta-tion in the gene for laminin γ-1, which eliminated just thebinding site for nidogen, died at birth with severe defectsin lung and kidney formation. The mutant portion of thelaminin γ-1 chain is thought to have no other functionthan to bind nidogen, and does not affect laminin struc-ture or its ability to assemble into the basal lamina.…
A single UASG regulates the expression of threegenes, all of which are adjacent: GAL7 and GAL10 asdescribed in Problem 8, and also GAL1.a. Would you expect these genes to be transcribedinto individual transcripts, or to be cotranscribed asone mRNA? Explain.b. How could you determine experimentallywhether each gene is transcribed separately orinstead that the three are cotranscribed into asingle mRNA?c. GAL1 and GAL10 are not only adjacent to eachother, but also are transcribed divergently with asingle UASG between them. Describe experimentsusing GFP and RFP transgenes that would allowyou to determine which of the four GAL4 bindingsites in this UASG element is (are) important for thetranscription of GAL1 and/or GAL10.
. An interesting mutation in lacI results in repressorswith 110-fold increased binding to both operator andnonoperator DNA. These repressors display a “reverse”induction curve, allowing β-galactosidase synthesis inthe absence of an inducer (IPTG) but partly repressingβ-galactosidase expression in the presence of IPTG. Howcan you explain this? (Note that, when IPTG binds a repressor, it does not completely destroy operator affinity,but rather it reduces affinity 110-fold. Additionally, ascells divide and new operators are generated by thesynthesis of daughter strands, the repressor must findthe new operators by searching along the DNA, rapidlybinding to nonoperator sequences and dissociating fromthem.)
The protein encoded by the cystic fibrosis gene is 1480amino acids long, yet the gene spans 250 kb. How is thisdifference possible?
A cloned gene fragment contains a regulatory element that isrecognized by a regulatory transcription factor. Previousexperiments have shown that the presence of a hormone resultsin transcriptional activation by this transcription factor. To studythis effect, you conduct an electrophoretic mobility shift assayand obtain the following results: Explain the action of the hormone.
To construct an “interactome” like the one shown inFigure 9-21, scientists identify all of the protein interactions in a particular tissue or cell type. Comparison ofinteractomes from human muscle versus human braintissue reveals very different patterns. If you were the scientist involved in this study, how would you explainthese results?
What is the length in AA’s of the LilP protein? Assume fMet is NOT CLEAVED.
Alternative splicing is a common mechanism for eukaryotes toexpand their repertoire of gene functions. At least one estimateindicates that approximately 50 percent of human genes usealternative splicing, and approximately 15 percent of diseasecausingmutations involve aberrant alternative splicing. Differenttissues show remarkably different frequencies of alternativesplicing, with the brain accounting for approximately 18 percentof such events. Why might some tissues engage in more alternative splicingthan others?
In addition to Tc1, the C. elegans genome contains otherfamilies of DNA transposons such as Tc2, Tc3, Tc4, andTc5. Like Tc1, their transposition is repressed in thegerm line but not in somatic cells. Predict the behaviorof these elements in the mutant strains where Tc1 is nolonger repressed due to mutations in the RNAi pathway.Justify your answer.
. a. Mice engineered to block expression of the geneencoding the telomerase protein age at a muchfaster rate than normal and have decreased lifespans. When expression of the telomerase proteinis turned back on in mice that are prematurely old,many negative effects of this aging are rapidly anddramatically reversed. Provide a possible explanation for these results.b. The results of these mouse experiments have ledsome researchers to propose that treatments thatcould lead to overexpression of the telomerase genemight serve as a “fountain of youth” leading to reversal of aging in humans. Why do you think weshould be very cautious about trying such treatments? Your argument should address why it mightbe advantageous to multicellular organisms for mostof their somatic cells not to express telomerase.
88Sequential binding of RNA polymerase II-TFIIF complex, TFIIE, and TFIIH completes ___________________ formation. A.pre-initiation complexb.TF recognition elementc.pre-elongation complexD.TATA binding complex 89Which of the following is the GDP-GTP exchange protein?A.EF-Tub.none of the abovec.EF-TsD.EF-G 90RNA polymerase II has 14 subunits. Yesorno